Irradiation which acts directly and produces the reactive oxygen radicals by ionizing water molecules, causes significant morbidity and mortality. The muscle is damaged by direct action, oxygen radicals and the alterations of microcirculation and metabolism after irradiation. The changes of SOD immunoreactivities in muscles of the rats after irradiation were observed. The ultrastructural changes of the irradiated muscles with the pretreatment of SOD (superoxide dismutase) or without were also investigated. A total of 60 healthy Sprague-Dawley male rats weighing from 200g to 250g were used as experimental animals. Under urethane (1.15g/kg. IP.2 times) anesthesia,30 Gy irradiation to lower extremities by PICKER-C9 Cobalt-60 teletherapy unit was done. 15,000 unit/kg of SOD was administered intraperitoneally 1 hour before irradiation. The experimental animals were sacrificed 1 day, 3 days, 7 days, 2 weeks and 4 weeks after irradiation. The superficial portions of the mid-belly of the rectus femoris muscles were obtained and sliced into portions, 2 mm in length, 1 mm in width and in thickness. The specimens were prepared by routine methods for the electron microscopic observation. All preparations were stained with uranyl acetate and lead citrate and observed with a Hitachi-600 electron microscope. The other parts of mid-belly of the rictus femoris muscles were sectioned in 14 micrometer thickness with cryostat at -20 degrees C. The immunoreactivities of SOD by use of antihuman Cu, Zn-and Mn-SOD antibodies were observed. The results were obtained as follows . 1. After irradiation, the immunoreactivities of SOD in the rictus femoris muscle were decreased. 2 weeks after irradiation, the immunoreactivities of Cu, Zn-SOD were trace, which was lowest.4 weeks after irradiation, the immunoreactivities were trace or weak. 1 day after irradiation, the immunoreactivities of Mn-SOD were trace, which was lowest. The immunoreactivities of Mn-SOD were increased gradually 4 weeks after irradiation, the immunoreactivities of Mn- SOD were moderate or weak. 2. The ultrastructural changes in the rectus femoris muscles of the rats were getting severer and severer after irradiation. 2 weeks after irradiation, unclear A band and I band, myofibrillolysis, increased and dilated cistemae of sarcoplasmic reticulum and mitochondria with dilated cristae and electron lucent matrix were seen. 4 weeks after irradiation, lysis of sarcomere and increased cisternae of sarcoplasmic reticulum were seen. 3. The ultrastructural changes in the rectus femoris muscles of the rats were getting worse and worse after 3 days of irradiation with the pretreatment of SOD. 2 weeks after irradiation with the pretreatment of SOD, myofibrillolysis, increased and dilated cisternae of sarcoplasmic reticulum and damaged mitochondria were seen. 4 weeks after irradiation with the pretreatment of SOD, the ultrastructures of rectus femoris muscles were recovered to normal. Consequently, after irradiation of 30 Gy, the immunoreactivities of SOD are decreased and SOD attenuates the reversible changes of ultrastructures in muscles.
Animals ; Antibodies ; Citric Acid ; Humans ; Lower Extremity ; Male ; Metabolism ; Microcirculation ; Mitochondria ; Mortality ; Muscles ; Quadriceps Muscle* ; Rats* ; Rats, Sprague-Dawley ; Reactive Oxygen Species ; Sarcomeres ; Sarcoplasmic Reticulum ; Superoxide Dismutase ; Urethane

It has been well known that ischemia reperfusion injury to skeletal muscle following an acute arterial occlusion causes significant morbidity and mortality. There are many causes of reperfusion injury, but the oxygen free radicals have a significant role. During ischemia the ATP is catalyzed to hypoxanthine anaerobically and hypoxanthine dehydrogenase is converted to xanthine oxidase under the presence of O2 resulting in the production of cytotoxic oxygen free radical, which are harmful to muscle. The reactivity of superoxide dismutase(SOD), one of the major antioxidant enzymes, is increased against the formation of the superoxide radical during reperfusion. SOD metabolyzes the superoxide radical to H2 O2 and O2.The severity of ischemic damage deports on the duration of muscle ischemia. The reversible changes in the muscle occur afar 2 hours of ischemia and recover within 24 hours after reperfusion. After 6 hours ischemia, irreversible damage occurs and causes necrosis of muscle. The authors performed the resent study to investigate the changes of Mn-SOD and the effects of allopurinol, the inhibitor of xanthine oxidase, by measuring the immunoreactivitiy of the ischemic reperfused rectus femoris muscle of rats after 2 hours and 6 hours ischemia and timely reperfusion. A total of 176 healthy spraque-Dawley rats weighing from 200 gm to 250 gm were used. Under urthane(3.0 gm/kg.,IP) anesthesia, a lower-abdominal incision was made and the left common iliac artery was ligated by using a vascular clamp for 2 hours and 6 hours. Rectus femoris muscle was obtained at 0 hour, 1 hour, 2 hours, 24 hours, and 48 hours after removal of the vascular clamp. The specimens were sectioned in 14micro miter thickness with a cryostat. The immunoreactivities of Mn-SOD were observed by using Mn-SOD antibodies. The result were as follows. 1. The immunoreactivies of Mn-SOD around sarcolemma were stronger than those on the sarcoplasm. 2. The immunoreactivities of Mn-S0D after 2 hours of ischemia increased to moderate or weak reactivities at 1 hour and 2 hours of reperfusion and returned to week or trace reactivities at 24 hours and 48 hours of reperfusion 3. The pretreatment of allopurinol decreased the immunoreactivies of Mn-SOD during reperfusion. The pattern of changes of SOD immunoreactivies were similar, but the range of changes significantly decreased. 4. The immunoreactivies of Mn-SOD after 6 hours of ischemia increased after 6 hours of ischemia increased after reperfusion and showed peak at 2 hours and 24 hours specimen. After 48 hours in the reperfused group, the reactivities slightly decreased. 5. After 6 hours in the ischemia-reperfused group, the pretreatment of allopurinol decreased the immunoreactivies of Mn-SOD during reperfusion, but the effects were weak. These results suggest that the immunoreactivities of the 6 hours ischemia reperfused group were higher than those of 2-hours ischemia reperfused group in the rectus femoris muscle of rats and that allopurinol pretreatment can be credited with decreasing ischemia reperfusion injury within a reversible period.
Adenosine Triphosphate ; Allopurinol ; Anesthesia ; Animals ; Antibodies ; Free Radicals ; Hypoxanthine ; Iliac Artery ; Ischemia ; Mortality ; Muscle, Skeletal ; Necrosis ; Oxygen ; Quadriceps Muscle* ; Rats* ; Reperfusion Injury* ; Reperfusion* ; Sarcolemma ; Superoxide Dismutase* ; Superoxides ; Xanthine Oxidase

BACKGROUND: Temporary interruption of blood flow to the liver is often unavoidable during operations for extensive injury of the liver or for major liver resection. Following ischemia- reperfusion, transient dysfunction of the liver occurs. It has been suggested that reactive oxygen metabolites play an important role in microvascular reperfusion injury. Superoxide dismutase (SOD) and dimethylthiourea (DMTU) are known to be antioxidants that scavenge oxygen free radicals to reduce microvascular reperfusion injury. This experiment studied the effect of SOD and DMTU on warm ischemia-reperfusion injury to the liver and compared inflow occlusion and hepatic vascular exclusion (HVE) after 20 minutes of ischemia. METHODS: One hundred fourteen healthy male Sprague-Dawley rats weighing around 250 g were used. The rats were divided into control (n=18) and experimental groups (n=96). The control groups included sham, SOD, and DMTU control groups. The experimental groups included inflow occlusion, SOD- pretreated inflow occlusion, DMTU-pretreated inflow occlusion, and inflow and outflow occlusion (HVE) groups. These 4 experimental groups had 24 rats each. The rats were sacrificed immediately, and at 24 hours, 48 hours, and 72 hours after reperfusion, and specimens were obtained from left anterior lobe of the liver. The specimens were prepared using routine methods for electron-microscope observations. RESULTS: The ultrastructures of the hepatocytes in all the experimental groups were similar to those of the normal control rats after just 20 minutes of ischemia. In the inflow occlusion group, dilatation and sacculation of the cisternae of the endoplasmic reticulum and mitochondria with many electron dense granules were observed in the hepatocytes after 24 hours of reperfusion. In the course of reperfusion, damage progressed until 72 hours after reperfusion. The HVE group showed more serious changes than the inflow occlusion group. The SOD- and the DMTU-treated groups showed clear attenuation of liver damage after 48 and 72 hours of reperfusion.CONCLUSION: The ultrastructural changes of hepatocytes after 20 minutes of ischemia became more prominent by prolonging the reperfusion time. The changes after hepatic inflow occlusion were less prominent than those after HVE. DMTU and SOD attenuated the injury to hepatocytes after warm ischemia-reperfusion.
Animals ; Antioxidants ; Dilatation ; Endoplasmic Reticulum ; Free Radicals ; Hepatocytes* ; Humans ; Ischemia ; Liver ; Male ; Mitochondria ; Oxygen ; Rats* ; Rats, Sprague-Dawley ; Reperfusion ; Reperfusion Injury* ; Superoxide Dismutase* ; Superoxides*

In skeletal muscles, oxygen free radicals generated during ischemia -reperfusion are known as inducers that cause cellular injury and apoptosis and contribute to the pathogenensis of reperfusion injury. Ischemia -reperfusion for 2 hours may cause reversible changes, while prolonged ischemia -reperfusion causes irreversible changes. Following ischemia -reperfusion, diverse signals are transduced to induce a variety of gene expression. Ischemic preconditioning, defined as brief episodes of ischemia and reperfusion, is known to provide protection from the consequences of prolonged ischemia followed by reperfusion. NF -kappa B is a transcription factor that activated during ischemic preconditioning and ischemia -reperfusion. It initiates inflammation through inducing transcription of proinflammatory, procoagulant and vasoactive gene, while mediates the expression of cytoprotective proteins that block apoptosis or inhibit inflammation. The present study was performed to study the change of NF -kappa B immunoreacitvity in rat anterior tibialis and soleus muscles in response to ischemia -reperfusion and preconditioning. Experimental animals, Sprague -Dawley rats (250 ~300 g), were divided into 6 groups; 1) control, 2) ischemic preconditioning, 3) 2 hours of ischemia, 4) 4 hours of ischemia, 5) 2 hours of ischemia after ischemic preconditioning, 6) 4 hours ischemia after ischemic preconditioning. For ischemic preconditioning, left common iliac artery was occluded three times for 5 minutes followed by 5 minutes of reperfusion using vascular clamp. Ischemia was done by occlusion of the same artery for 2 or 4 hours. The specimens of tibialis anterior and soleus muscles were obtained 0, 1, 3, 6, and 24 hours after onset of reperfusion. The specimens were paraffin sectioned at 6 micrometer and NF -kappa B expression was examined using immunohistochemical methods. The results obtained were as follows : 1. In normal control group, immunoreactivity of NF -kappa B was moderate to strong in tibialis anterior muscles and weak in soleus muscles. 2. In tibialis anterior, immunoreactivity of NF -kappa B was decreased in 2 and 4 hours of ischemia comparede with normal control group. In soleus muscle, immunoreactivity of NF -kappa B was decreased in 2 hours of ischemia but it was comparable to that of normal control group in 4 hours of ischemia. 3. Ischemia for 4 hours induced more remarkable change in NF -kappa B immunoreactivity than that for 2 hours. 4. After ischemic preconditioning, changes in NF -kappa B immunoreactivity after 2 and 4 hours of ischemia were decreased compared with normal control group. 5. In ischemia for 2 and 4 hours, changes in NF -kappa B immunoreactivity of tibialis anterior muscles were more severe than that of soleus muscles. These results suggest that in the skeletal muscle, changes in NF -kappa B immunoreactivity of 4 hours of ischemia were more remarkable than that of 2 hours ischemia, and changes in NF -kappa B of tibialis anterior muscles were more remarkable than that of soleus muscles. Ischemic preconditiong attenuated the alteration of the NF -kappa B immunoreactivity induced by ischemia -reperfusion in the muscles.
Animals ; Apoptosis ; Arteries ; Free Radicals ; Gene Expression ; Iliac Artery ; Inflammation ; Ischemia ; Ischemic Preconditioning ; Muscle, Skeletal ; Muscles* ; Oxygen ; Paraffin ; Rats* ; Reperfusion ; Reperfusion Injury ; Transcription Factors

A brief episode of ischemia and reperfusion termed 'ischemic preconditioning' has been established as rendering muscle tolerance to damage during a subsequent prolonged ischemia. The effects of ischemic preconditioning in the cardiac muscle is related to the stimulation of adenosine A1 receptor and the opening of KATP channel. The effect and mechanism of ischemic preconditioning in the skeletal muscle is not known clearly. The author performed the present study to investigate the effect and the mechanisms of ischemic preconditioning by measuring the SOD immunoreactivities on timely reperfused ischemic muscles. The healthy Sprague -Dawley rats weighing from 200 g to 250 g were used as experimental animals. Under pentobarbital (50 mg/kg) anesthesia, lower abdominal incision was done and left common iliac artery was ligated by using vascular clamp for 2 hours. Rectus femoris muscles were obtained at 0 hour, 1 hour, 2 hours, 6 hours, 12 hours, 24 hours, 48 hours and 72 hours of reperfusion. The group of ischemic preconditioning underwent three episodes of 5 minute occlusion and 5 minute reperfusion of common iliac artery followed by 2 hours of ischemia and timely reperfusion. Adenosine (50 microgram/kg) or pinacidil (1 mg/kg) were administered intravenously before ischemia and 2 hours of ischemia and timely reperfusion was done. 10 microM thick cryosections in all groups were obtained. The immunoreactivities of SOD were observed by use of antihuman Cu,Zn -and Mn -SOD antibodies. The results obtained were as follows. 1. The immunoreactivities of SOD in the rectus femoris muscles of rats increased after ischemic preconditioning. The patterns of the changes in immunoreactivities of Cu, Zn -and Mn -SOD were similar at the muscle fibers with large section area or small section area. 2. After the treatment of adenosine, the immunoreactivities of Cu, Zn -SOD in the group of 2 hours and 24 hours reperfusion and the immunoreactivities of Mn -SOD in the group of 24 hours reperfusion increased. After the treatment of pinacidil, the immunoreactivities of Mn - SOD increased and the immunoreactivities of Cu, Zn -SOD are similar to normal control rat. 3. After 2 hours of ischemia the immunoreactivities of SOD were similar to normal control rat. The immunoreactivities of Cu, Zn -SOD in the group of 1 hour, 2 hours and 24 hours reperfusion and those of Mn -SOD in all groups of reperfusion increased. 4. In the group of 2 hours ischemia and timely reperfusion with ischemic preconditioning, the immunoreactivities of SOD in the muscle fiber with large section area decreased and those of SOD in the muscle fibers with small section area increased in comparison with the group of 2 hours and timely reperfusion. The pattern of change between immunoreactivities of Cu,Zn -and Mn -SOD in each muscle fiber were similar. 5. After the treatment of adenosine, the immunoreactivities of SOD increased in the group of 1 hour, 2 hours, 6 hours and 12 hours reperfusion. After the treatment of pinacidil, the immunoreactivities of SOD increased in the group of 1 hour, 2 hours, 6 hours, 12 hours and 24 hours reperfusion. Consequently, these results suggest that the immunoreactivities of SOD increase after 2 hours of ischemia and timely reperfusion with ischemic preconditioning. The effect of ischemic preconditioning is related to opening of KATP channel partly.
Adenosine ; Anesthesia ; Animals ; Antibodies ; Iliac Artery ; Ischemia* ; Ischemic Preconditioning ; Muscle, Skeletal ; Muscles* ; Myocardium ; Pentobarbital ; Pinacidil* ; Quadriceps Muscle* ; Rats* ; Receptor, Adenosine A1 ; Reperfusion*

Ischemic preconditioning (IP), short pre-treatment sublethal ischemia, induces a state of protection against subsequent prolonged ischemia-reperfusion. The purpose of this study was to investigate the expression of HO-1, HSP70, and iNOS proteins in the liver subjected to the courses of reperfusion after repetitive cycles of remote IP in the rat. Using thirty five week-old rats, the remote preconditioning was undertaken by vascular clamp occlusion of blood flow to one hindlimb, with 3 and 10 cycles of 5 minutes occlusion followed by 5 minutes reperfusion. The liver was removed 0, 3, 6, 24, and 72 hours of reperfusion after remote IP and assayed by immunohistochemical staining and Western blotting analyses for anti-HO-1, anti-HSP70, and anti-iNOS antibodies. The expression of HO-1 in rat liver increased at 72 hours of reperfusion groups after 3 and 10 cycles of remote IP, compared with normal control groups. The expression of HSP70 in rat liver increased at 6 hours of reperfusion groups after 3 cycles of remote IP, compared with normal control groups. The expression of HSP70 in rat liver increased at 0 hour of reperfusion groups after 10 cycles of remote IP, compared with normal control groups and decreased at 24 and 72 hours of reperfusion groups. The expression of iNOS in rat liver increased at 24 hours of reperfusion groups, but decreased at 72 hours of reperfusion groups after 3 and 10 cycles of remote IP, compared with normal control groups. In summary, these results showed that at early phase of reperfusion after remote IP, HSP70 expression was increased in rat liver. However, at 72 hrs of reperfusion after remote IP, HO-1 expression was increased and iNOS expression was decreased in rat liver.
Animals ; Blotting, Western ; Hindlimb ; Ischemia ; Ischemic Preconditioning ; Liver ; Proteins ; Rats ; Reperfusion

We studied the distribution patterns of perforating branch of superficial circumflex iliac artery for flap surgery in Korean. Fifty one thighs from 34 Korean cadavers (17 males/ 17 females) were dissected and standard points were determined as follows: point of anterior superior iliac spine (A), point of pubic tubercle (B), cross point of the line AB and femoral artery (FA), cross point of the femoral artery and the sartorius muscle (FAS), beginning point of superficial circumflex iliac artery (O), and perforating point of superficial circumflex iliac artery (P). We measured the distance and the angles between the standard points. Each frequency of superficial circumflex iliac artery from femoral artery and superficial epigastric artery is 69.6% and 30.4% respectively. The mean distance between the beginning point of superficial circumflex iliac artery (O) and the point A was 7.3+/-1.3 cm and the mean distance between the point O and the point B was 5.7+/-0.6 cm. The angle from line OA to line AB was 17.9+/-8.0 degrees and The angle from line OB to the line AB was 24.9+/-5.1 degrees. The mean distance between the perforating point for superficial circumflex iliac artery (P) and the point A was 6.3+/-2.4 cm and the mean distance between the point P and the point B was 8.3+/-2.7 cm. The angle from line PA to line AB was 33.4+/-18.3 degrees and the angle from line PB to the line AB was 24.5+/-14.3 degrees. Consequently, the pattern of distribution of superficial circumflex iliac arteries, obtained in this study, will provide useful anatomical backgrounds for the superficial circumflex iliac artery flap surgery in Korean.
Cadaver ; Epigastric Arteries ; Femoral Artery ; Iliac Artery* ; Spine ; Thigh

PURPOSE: Prolonged hepatic ischemia followed by reperfusion in surgery or transplantation results in severe cell death. Apoptosis is one type of cell death and occurs under various conditions. Apoptosis differs from necrosis not only morphologically but also in the mediators and mechanism of injury. It has been recently recognized that oxygen-free radicals are major mediators of apoptosis during ischemia/reperfusion. It was reported that pretreatment with a radical scavenger, such as catalase or superoxide dismutase (SOD) attenuated the apoptotic cell death and that old animals showed a higher catalase, SOD, glutatione peroxidase activity in their livers than young rats. This study was designed to characterize the types of cells within the liver and the extent to which those cells undergo apoptosis during ischemia/reperfusion in rats of different ages and to investigate the effect of dimethylthiourea (DMTU), a scanvenger of reactive hydroxyl radicals, on the induction of apoptosis in old rats. METHODS: Young male Sprague-Dawley rats at 5 weeks of age weighing about 200 gm and old rats at 15 weeks of age weighing about 450 gm were subjected to 30-minute ischemia. Liver ischemia was performed by inflow occlusion. Another group of old rats was injected with DMTU before the clamping. The rats were sacrificed immediately and at 1, 3, and 24 hour(s) after reperfusion. The specimens were prepared using in-situ staining for apoptotic cell and bodies by using terminal deoxytransferase-mediated dUTP- biotin nick-end labelling (TUNEL) methods. RESULTS: The number of apoptotic sinusoidal endothelial cells was larger than the number of hepatocytes during ischemia/reperfusion. The apoptosis of hepatocytes significantly increased at 1 hour and at 3 hours in the young group. Although the number of cells in the old group was lower than that in young rats, an increase of TUNEL positive hepatocytes cells was noted at 1 hour. There was significant increase in the DMTU-pretreated old rats until 24 hours afterreperfusion. The number of apoptotic sinusoidal endothelial cells was noticeably higher in DMTU- pretreated old rats than you only defined two groups previously: old and young in the other group. In young rats, but not old rats, an increase of positive sinusoidal endothelial cells was observed at 1 hours after reperfusion. CONCLUSION: These results suggested that old rats have more resistance to ischemia/reperfusion injury than young rats and that DMTU dose not attenuate apoptosis of sinusoidal endothelial cells after ischemia/reperfusion, but dose attenuate apoptosis of hepatocytes in the liver.
Animals ; Apoptosis* ; Biotin ; Catalase ; Cell Death ; Constriction ; Endothelial Cells ; Hepatocytes ; Humans ; In Situ Nick-End Labeling ; Ischemia* ; Liver* ; Male ; Necrosis ; Peroxidase ; Rats* ; Rats, Sprague-Dawley ; Reperfusion* ; Superoxide Dismutase

Free radicals, formed by ionization of water molecules, cause significant increase of morbidity and mortality in irradiated humans. The skeletal muscle is relatively radio-resistant because of its few content of proliferating cells. But the incidence and severity of muscular damage depends on the dose of radiation and time lapse. This study is aimed to investigate the ultrastructural changes and the effect of radiation and DMTU on two muscles, the tibialis anterior and the soleus muscle; the former is dominantly composed of white muscles while the latter is mainly composed of red muscles. Each muscle also show differences in energy production and distribution of capillaries. The male Sprague-Dawley rats weighing from 200 g to 250 g were used as experimental animals. Under urethane(1.15 g/kg, i.p.) anesthesia, 30Gy irradiation to lower extremities with PICKER-C9 cobalt 60 teletherapy unit was done. DMTU(500 mg/kg, i.p.) was administered 1 hour prior to irradiation. The animals were sacrificed 1 day, 3 days, 7 days, 2 weeks, and 4 weeks after irradiation. The muscular tissues in midbelly of tibialis anterior and the soleus muscles were obtained and sliced into 2 mm in length, 1 mm in width and thickness. The specimens were prepared by routine method for electron microscopy. The results obtained were as follows: 1. Widening of interfibrillar space, mitochondrial changes of eletron-lucent matrix and dilated cristae, and cisternal dilatation of sarcoplasmic reticulum were observed in both muscles after irradiation. More severe ultrastructural changes with time course were observed by 2 weeks. But those were recovered to normal at 4 weeks after irradiation. 2. More severe ultrastructural changes in soleus were observed 1 and 3 days after irradiation, and in tibialis anterior at 7 days and 2 weeks. Those findings were associated with reduction of glycogen contents in the myofibers of both muscles. 3. Widening of intermyofibrillar space, mitochondrial changes of electron-lucent matrix and indistinct cristae, and cisternal dilatation of sarcoplasmic reticulum were observed in both muscles after DMTU treatment. 4. Pretreatment of DMTU attenuated the ultrastructural changes induced by irradiation. Those were recoved normally by 2 weeks. Consequently, DMTU attenuates the ultrastructural changes in tibialis anterior and soleus muscle after irradiation. The more severe morphological changes in soleus muscle at 1 day and 3 days, and in tibialis anterior at 7 days and 2 weeks after irradiation are associated with the reduction of glycogen contents.
Anesthesia ; Animals ; Capillaries ; Cobalt ; Dilatation ; Free Radicals ; Glycogen ; Humans ; Incidence ; Lower Extremity ; Male ; Microscopy, Electron ; Mortality ; Muscle, Skeletal ; Muscles* ; Rats* ; Rats, Sprague-Dawley ; Sarcoplasmic Reticulum

Fibronectin (FN) is a major extracellular matrix glycoprotein, highly expressed in developing rat lungs. Several observations suggest that it play an important role in many developmental processes of animals. In vitro, FN can affect the adhesion, migration, proliferation, differentiation, and even apoptosis of various cell types. This study was undertaken to describe the distribution and localizations of fibronectin in the alveolar septum of lungs and liver lobules after CS gas exposure to experimental rats. The experimental rats (Sprague-Dawley strain), weighing 150~200 gm were sacrificed at 6 hours, 12 hours, 24 hours, 48 hours and 72 hours after CS gas exposure. The specimens of lung and liver were prepared for fibronectin immunoreactions of alveolar septa and liver lobules on experimental group, and for fibronectin reactions on the cytoplasm of type I alveolar cells, type II alveolar cells, fibroblasts, alveolar macrophages and interstitium in alveolar septa of lungs. All of specimens for immune reactions were observed with light and electron microscopes. The results obtained were as follows. 1. The liver lobules showed mild fibronectin reactions at the 6 hours and 12 hours after CS gas exposure. 2. The alveolar macrophages revealed strong fibronectin reactions. But alveolar septa showed weak FN reactions at 6 hours after CS gas exposure. 3. At 12 hours and 24 hours after CS gas exposure, the interstitial pneumonitis were seen in the lung alveoli. The gold particles were increased in the cells of alveolar septa, weak fibronectin reactions were revealed in the alveolar septum. 4. At 48 hours and 72 hours after CS gas exposure, FN reactions of alveolar septa were moderate, and the gold particles in the alveolar cells were markedly decreased. These results suggest that CS gas exposure to rats induces the increase of the fibronectin in lung and liver.
Animals ; Apoptosis ; Cytoplasm ; Extracellular Matrix ; Fibroblasts ; Fibronectins* ; Glycoproteins ; Liver* ; Lung Diseases, Interstitial ; Lung* ; Macrophages, Alveolar ; Rats*